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Kaech, H.

Publications and source records attributed to Kaech, H..

3 recordsLinked to original sources

Dual RNA-seq in an aphid parasitoid reveals plastic and evolved adaptation to symbiont-conferred resistance

Coevolving taxa offer the opportunity to study the genetic basis of rapid reciprocal adaptation. We have used experimental evolution to examine adaptation in the parasitoid wasp Lysiphlebus fabarum to resistance conferred by the protective endosymbiont Hamiltonella defensa in its aphid host Aphis fabae. To examine a key stage in parasitoid infection, we have used RNA-seq to study gene expression in 4-5 day old parasitoid larvae contained in still living aphids. With this dual RNA-seq we can simultaneously view expression in individual experimentally evolved parasitoids and the aphids that house them. This gives a view of the sweeping changes in both taxa accompanying successful or unsuccessful infections. Among successful larvae, we find that experimentally evolved populations adapted to H. defensa-protected hosts differ in the expression of genes that include putative toxins and genes to cope with stress. These differences remain even when the larvae are developing in aphids possessing no defensive endosymbionts, suggesting that they are genetically based. In contrast, plastic responses between parasitoids reared in hosts with and without H. defensa are relatively small. Although aphids rely largely on their secondary endosymbionts for defense against parasitoids, we identify expression differences in aphids housing different parasitoid phenotypes. Together, these results demonstrate that wild parasitoid populations possess the genetic variation for rapid adaptation to host resistance, resulting in genetically based differences in gene expression that increase their success in parasitizing symbiont-protected host aphids.

evolutionary biology↗

Non-random associations of maternally transmitted symbionts in insects: The roles of drift versus co-transmission and selection

Virtually all higher organisms form holobionts with associated microbiota. To understand the biology of holobionts we need to know how species assemble and interact. Controlled experiments are suited to study interactions between particular symbionts, but they can only inform about a tiny portion of the diversity within each species. Alternatively, interactions can be inferred from associations among symbionts in the field that are more or less frequent than expected under random assortment. However, random assortment may not be a valid null hypothesis for maternally transmitted symbionts in finite populations, where drift alone can result in associations. Here we report results from a European field survey of endosymbionts in the pea aphid (Acyrthosiphon pisum), and we develop a model to study the effect of drift on symbiont associations under different population sizes, considering varying rates of horizontal and maternal transmission. The model showed that even though horizontal transmissions and maternal transmission failures tend to randomise symbiont associations, drift can induce significant departures from random assortment, at least in moderate-sized populations. Based on these results, we carefully interpret our field survey and we re-visit the association between Spiroplasma and Wolbachia in Drosophila neotestacea reported by Jaenike et al. (2010). For this and for several significant associations between symbionts in European pea aphids we conclude that under reasonable assumptions of effective population size, they are indeed likely to be maintained by biased co-transmission or selection. Our study shows that formulating appropriate null expectations can strengthen the biological inference from co-occurrence patterns in the field.

ecology↗

Ancestral perinatal obesogen exposure results in a transgenerational thrifty phenotype in mice

Ancestral environmental exposures to non-mutagenic agents can exert effects in unexposed descendants. This transgenerational inheritance has significant implications for understanding disease etiology. The obesogen hypothesis proposes that exposure to obesogenic chemicals can lead to increased adiposity, in vivo. Here we show that exposure of F0 mice to the obesogen tributyltin (TBT) throughout pregnancy and lactation predisposes unexposed F4 male descendants to obesity when dietary fat is increased. Analyses of body fat, plasma hormone levels, and visceral white adipose tissue DNA methylome and transcriptome collectively indicate that the F4 obesity is consistent with a leptin resistant, \"thrifty phenotype\". Ancestral TBT exposure induces global changes in DNA methylation together with altered expression of metabolism-relevant genes when the F4 animals were exposed to dietary challenges. Analysis of chromatin accessibility in F3 and F4 sperm reveal significant differences between control and TBT groups and significant similarities between F3 and F4 TBT groups that overlap with areas of differential methylation in F4 adipose tissue. Taken together, our data suggest that ancestral TBT exposure induces changes in higher order chromatin organization transmissible through meiosis and mitosis.\n\nNon-technical summaryAncestral obesogen exposure in mice causes obesity in untreated F4 male descendants by inducing heritable changes in genome architecture that predispose these animals to become obese when dietary fat is increased modestly. This result is consistent with these animals having a leptin-resistant, \"thrifty\" phenotype

developmental biology↗